Sonnenblick M, Rosin A J
Postgrad Med J. 1986 Jun;62(728):449-52. doi: 10.1136/pgmj.62.728.449.
The biochemical features of severe hyponatraemia due to thiazide administration in 7 non-oedematous patients were compared with those in hyponatraemia due to frusemide. Hypouricaemia has been shown to occur in hyponatraemia due to the syndrome of inappropriate antidiuretic hormone activity and this was measured along with fractional uric acid clearances in all the patients. Five of the patients had been on thiazides (or hydrochlorothiazide with amiloride) for only a few days to a few weeks. Fractional uric acid clearance was elevated and serum uric acid levels were low in five of them and returned to the normal range on restoration of serum sodium to normal. By contrast, the patients on frusemide did not show any abnormality in fractional uric acid clearance at any stage. These results are consistent with excess ADH activity as having caused hyponatraemia induced by thiazides in 5 of the 7 cases, whereas frusemide caused a sodium depletion syndrome. Treatment in the former cases is by water restriction, and in frusemide-induced salt depletion by saline supplementation.
将7例非水肿性患者因噻嗪类药物导致的严重低钠血症的生化特征与因速尿导致的低钠血症患者的生化特征进行了比较。低尿酸血症已被证明会在抗利尿激素分泌异常综合征导致的低钠血症中出现,并且在所有患者中都对其进行了测量,同时还测量了尿酸清除率。其中5例患者服用噻嗪类药物(或氢氯噻嗪与阿米洛利合用)仅数天至数周。其中5例患者的尿酸清除率升高,血清尿酸水平降低,血清钠恢复正常后尿酸水平恢复到正常范围。相比之下,使用速尿的患者在任何阶段的尿酸清除率均未显示任何异常。这些结果表明,7例中有5例噻嗪类药物导致的低钠血症是由抗利尿激素活性过高引起的,而速尿则导致了钠耗竭综合征。前一种情况的治疗方法是限制水分摄入,而速尿引起的盐耗竭则通过补充生理盐水来治疗。